Gene expression profile of CD11b+ Gr1+ Myeloid derived suppressor cells isolated from tumor microenviroment and bone marrow oat different stages of tumor bearing animals and control animals.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE236469 | GEO | 2024/01/13
REPOSITORIES: GEO
Similar Datasets
Project description:Gene expression profile of CD11b+ Gr1+ Myeloid derived suppressor cells isolated from tumor microenviroment and bone marrow oat different stages of tumor bearing animals and control animals.
| PRJNA991435 | ENA
Project description:Myeloid derived suppressor cells (MDSCs) are an immunosuppressive population of immature myeloid cells found in advanced stage cancer patients and mouse tumor models. To identify potential genes playing essential role in MDSC biology, we have conducted microarray analysis of gene expression in MDSCs from esophageal tumor-bearing mice, compared to immature myeloid cells from healthy littermate control mice. In this dataset, we include the expression data obtained from sorted splenic CD11b+Gr1+ cells from tumor-bearing L2-Cre;p120f/f mice, compared to healthy littermate controls. Using these data, we have identified 964 genes showing differential expression between the two groups. Among these was the Cd38 gene, which was among the genes most upregulated in MDSCs from tumor-bearing mice. 9 total samples were analyzed: 6 sample from experimental tumor-bearing mice and three pooled samples from control mice. Gene expression difference was determined by univariate test (two-sample t-test) with multivariate permutation test (10,000 random permutations). A cut-off p-value of less than 0.001 and minimum 2-fold expression change were used to identify genes with significant expression differences between the two groups.
2015-08-31 | E-GEOD-71706 | biostudies-arrayexpress
Project description:Myeloid derived suppressor cells (MDSCs) are an immunosuppressive population of immature myeloid cells found in advanced stage cancer patients and mouse tumor models. To identify potential genes playing essential role in MDSC biology, we have conducted microarray analysis of gene expression in MDSCs from esophageal tumor-bearing mice, compared to immature myeloid cells from healthy littermate control mice. In this dataset, we include the expression data obtained from sorted splenic CD11b+Gr1+ cells from tumor-bearing L2-Cre;p120f/f mice, compared to healthy littermate controls. Using these data, we have identified 964 genes showing differential expression between the two groups. Among these was the Cd38 gene, which was among the genes most upregulated in MDSCs from tumor-bearing mice.
2015-08-31 | GSE71706 | GEO
Project description:Myeloid derived suppressor cells (MDSCs) are an immunosuppressive population of immature myeloid cells found in advanced stage cancer patients and mouse tumor models. We have identified Cd38 gene as potentially playing an essential role in MDSC biology. To determine the diffences between CD38high and CD38 low MDSCs from tumor-bearing mice, we have conducted this microarray. In this dataset, we include the expression data obtained from sorted splenic CD38high CD11b+Gr1+ cells from tumor-bearing L2-Cre;p120f/f mice, compared to CD38low CD11b+Gr1+ cells from the same mice. Using these data, we have detected differential expression of 498 genes . The Nos2 gene was among the genes most upregulated in CD38high MDSCs.
2015-08-31 | GSE71705 | GEO
Project description:Myeloid derived suppressor cells (MDSCs) are an immunosuppressive population of immature myeloid cells found in advanced stage cancer patients and mouse tumor models. We have identified Cd38 gene as potentially playing an essential role in MDSC biology. To determine the diffences between CD38high and CD38 low MDSCs from tumor-bearing mice, we have conducted this microarray. In this dataset, we include the expression data obtained from sorted splenic CD38high CD11b+Gr1+ cells from tumor-bearing L2-Cre;p120f/f mice, compared to CD38low CD11b+Gr1+ cells from the same mice. Using these data, we have detected differential expression of 498 genes . The Nos2 gene was among the genes most upregulated in CD38high MDSCs. 8 total samples were analyzed: 3 pairs of CD38high and CD38 low MDSCs (coming from individual mice), as well a pair of CD38high and CD38low pulled MSDCs (splenocytes from 3 mice were pulled together for sorting to increase yields). Gene expression difference was determined by univariate test (two-sample t-test) with multivariate permutation test (10,000 random permutations). A cut-off p-value of less than 0.001 and minimum 2-fold expression change were used to identify genes with significant expression differences between the two groups.
2015-08-31 | E-GEOD-71705 | biostudies-arrayexpress
Project description:BackgroundChemokines are involved in multiple aspects of pathogenesis and cellular trafficking in tumorigenesis. In this study, we report that the latest member of the C-X-C-type chemokines, CXCL17 (DMC/VCC-1), recruits immature myeloid-derived cells and enhances early tumor progression.Methodology/principal findingsCXCL17 was preferentially expressed in some aggressive types of gastrointestinal, breast, and lung cancer cells. CXCL17 expression did not impart NIH3T3 cells with oncogenic potential in vitro, but CXCL17-expressing NIH3T3 cells could form vasculature-rich tumors in immunodeficient mice. Our data showed that CXCL17-expressing tumor cells increased immature CD11b(+)Gr1(+) myeloid-derived cells at tumor sites in mice and promoted CD31(+) tumor angiogenesis. Extensive chemotactic assays proved that CXCL17-responding cells were CD11b(+)Gr1(high)F4/80(-) cells (? 90%) with a neutrophil-like morphology in vitro. Although CXCL17 expression could not increase the number of CD11b(+)Gr1(+) cells in tumor-burdened SCID mice or promote metastases of low metastatic colon cancer cells, the existence of CXCL17-responding myeloid-derived cells caused a striking enhancement of xenograft tumor formation.Conclusions/significanceThese results suggest that aberrant expression of CXCL17 in tumor cells recruits immature myeloid-derived cells and promotes tumor progression through angiogenesis.
| S-EPMC3430639 | biostudies-literature
Project description:During pregnancy, the ETS transcription factor ELF5 establishes the milk-secreting alveolar cell lineage by driving a cell fate decision of the mammary luminal progenitor cell. In breast cancer, ELF5 is a key transcriptional determinant of tumor subtype and has been implicated in the development of insensitivity to anti-estrogen therapy. In the mouse mammary tumor virus-Polyoma Middle T (MMTV-PyMT) model of luminal breast cancer, induction of ELF5 levels increased leukocyte infiltration, angiogenesis, and blood vessel permeability in primary tumors and greatly increased the size and number of lung metastasis. Myeloid-derived suppressor cells, a group of immature neutrophils recently identified as mediators of vasculogenesis and metastasis, were recruited to the tumor in response to ELF5. Depletion of these cells using specific Ly6G antibodies prevented ELF5 from driving vasculogenesis and metastasis. Expression signatures in luminal A breast cancers indicated that increased myeloid cell invasion and inflammation were correlated with ELF5 expression, and increased ELF5 immunohistochemical staining predicted much shorter metastasis-free and overall survival of luminal A patients, defining a group who experienced unexpectedly early disease progression. Thus, in the MMTV-PyMT mouse mammary model, increased ELF5 levels drive metastasis by co-opting the innate immune system. As ELF5 has been previously implicated in the development of antiestrogen resistance, this finding implicates ELF5 as a defining factor in the acquisition of the key aspects of the lethal phenotype in luminal A breast cancer.
| S-EPMC4696735 | biostudies-literature
Project description:BackgroundHistological examinations of MMTV-Wnt1 tumors reveal drastic differences in the tumor vasculature when compared to MMTV-Her2 tumors. However, these differences have not been formally described, nor have any angiogenic factors been implicated to be involved in the Wnt1 tumors.Methodology/principal findingsHere, we show that MMTV-Wnt1 tumors were more vascularized than MMTV-Her2 tumors, and this correlated with significantly higher expression of a CXC chemokine, stromal cell-derived factor-1 (SDF1/CXCL12) but not with VEGFA. Isolation of various cell types from Wnt1 tumors revealed that SDF1 was produced by both tumor myoepithelial cells and stromal cells, whereas Her2 tumors lacked myoepithelial cells and contained significantly less stroma. The growth of Wnt1 tumors, but not Her2 tumors, was inhibited by a neutralizing antibody to SDF1, but not by neutralization of VEGFA. Anti-SDF1 treatment decreased the proportion of infiltrating Gr1(+) myeloid cells in the Wnt1 tumors, which correlated with a decrease in the percentage of endothelial cells. The involvement of Gr1(+) cells was evident from the retardation of Wnt1 tumor growth following in vivo depletion of these cells with an anti-Gr1-specific antibody. This degree of inhibition on Wnt1 tumor growth was comparable, but not additive, to the effect observed with anti-SDF1, indicative of overlapping mechanisms of inhibition. In contrast, Her2 tumors were not affected by the depletion of Gr1(+) cells.Conclusions/significanceWe demonstrated that SDF1 is important for Wnt1, but not for HER2, in inducing murine mammary tumor and the role of SDF1 in tumorigenesis involves Gr1(+) myeloid cells to facilitate growth and/or angiogenesis.
| S-EPMC2801592 | biostudies-literature
Project description:We sought to identify genes that are differentially regulated in CD11b+Gr1+ cells after tumor challenging. Mice were challenged with LLC-RFP cells (5×10^6 cells, subcutaneous injection) for 9 days. Single cell suspensions were prepared from lungs of both tumor challenged and control wild type mice and stained with antibodies against CD11b and Gr1. Approximately 1×10^5 CD11b+GR1+ myeloid progenitor cells were sorted by FACS (Aria II, BD Bioscience). Total RNA was extracted from the sorted cells for microarray analysis. In this dataset, we include the expression data of CD11b+Gr1+ cells obtained from both control wild type and tumor challenged mice. These data were used to obtain 22 genes that are upregulated in response to tumor challenging. We analyzed 3 samples from control mice and 2 samples tumor challenged mice. The mean values of the groups were used in the analysis. Genes that were upregulated >2 fold were sorted out and generate the table in the Matrix datasheet.
2012-01-01 | E-GEOD-20180 | biostudies-arrayexpress
Project description:We sought to identify genes that are differentially regulated in CD11b+Gr1+ cells after tumor challenging. Mice were challenged with LLC-RFP cells (5×10^6 cells, subcutaneous injection) for 9 days. Single cell suspensions were prepared from lungs of both tumor challenged and control wild type mice and stained with antibodies against CD11b and Gr1. Approximately 1×10^5 CD11b+GR1+ myeloid progenitor cells were sorted by FACS (Aria II, BD Bioscience). Total RNA was extracted from the sorted cells for microarray analysis. In this dataset, we include the expression data of CD11b+Gr1+ cells obtained from both control wild type and tumor challenged mice. These data were used to obtain 22 genes that are upregulated in response to tumor challenging.
2012-01-01 | GSE20180 | GEO